Normal Eye with Sudden Vision Loss

Dofi Pebriadi & Yusuf HarkianI11109068 – I11109097

Normal Eye with Sudden Vision Loss

• Sudden loss of vision associated with eye pain or headache in the white non-inflamed eye needs urgent attention as it may be due to sight or even life-threatening illness.

TopicOptic Neuritis

Retina Detachment

Central Retinal Arteri Occlusion

Central Retinal Vena Occlusion

Viterous Hemorragic

Toxic Ambliopia

Histeria

etc

OPTIC NEURITIS

Optic Neuritis

• An inflammation of the optic nerve that may occur within the globe (papillitis) or posterior to it ( retrobulbar optic neuritis).

• Most frequently in adults between the ages of 20 and 45.

• 20-40 % of all patients with optic neuritis develop diffuse encephalitis (multiple sclerosis).

• Papilitis anterior part, nerve is inflammed, optic disc will appear swollen.

• Retrobulbar neuritis behind the globe (i.e. the retrobulbar part of the nerve), sometimes didn’t look inflamation

Etiologi

• Papillitis.– Inflammatory processes: Lyme disease, malaria, and syphilis, and

manifestations in the optic nerve of inflammation of the orbit, paranasal sinuses, or base of t he sk ull.

– Autoimmune disorders: lupus erythematosus, polychon-dritis, regional enteritis (Crohn’s disease), ulcerative c olitis, nodular panarteritis, and Wegener’s granulomatosis.

– Toxic damage due to agents such as methanol, l ead, Myambutol (ethambu-tol hydrochloride), and chloramphenicol. In 70 % of these cases, the cause is not determined .

• Retrobulbar optic neuritis. – The primary causes: demyelinating diseases of the central nervous

system such as dif fuse encephalitis.

Symptom

• The cardinal symptom is sudden loss of vision, which may occasionally be accompanie d by fever ( Uhthof f symptom).

• Pain that increases in extreme positions of gaze when pressure is applied to the globe.

• Reduced perception of color intensity.

• The field of vision is typically impaired by a central scotoma, paracentral scotomas, a centrocecal scotoma involving the macula and blind spot, and wedge-shaped visual field defects up to and including complete blindness.

Diagnosis

• Papillitis include edema and hyperemia of the head of the optic nerve. This flat-tens the optic cup and obscures the margin of the optic disk. Bleeding at the margin of the optic disk may or may not be present.

• The optic disk will appear normal in retrobulbar optic neuritis.

Treatment

• Papilitis and neuritis retrobulbar have a same medication Corticosterioid.

• Abtibiotik to treat infection as a cause.

RETINAL DETACHMENT

• Separation of the neurosensory retina from the underlying retinal pigment epithelium, to which normally it is loosely attached.

• This can be classified into 4 types:– Rhegmatogenous retinal detachment results from a tear, i.e., a

break in the retina. Presdipotition in trauma and myopic.– Tractional retinal detachment results from traction, i.e., from

vitreous strands that exert tensile forces on the retina– Exudative retinal detachment is caused by fluid. Blood, lipids, or

serous fluid accumulates between the neurosensory retina and the retinal pigment epithelium. Coats’ disease is a typical example.

– Tumor-related retinal detachment.

Symtoms

• Retinal detachment can remain asymptomatic for a long time.

• In the stage of acute posterior vitreous detachment– flashes of light (photopsia) and floaters,– black points that move with the patient’s gaze. – Blood from this vessel will then enter the vitreous body. “black

rain,” numerous slowly falling small black dots .– Dark shadow in the visual field. The patient will perceive a falling

curtain or a rising wall, depending on whether the detachment is superior or inferior.

– A break in the center of the retina (macula is involved ) sudden and significant loss of visual acuity

Diagnostic• Ofthalmoscope : retina white and edematous and will lose its

transparency.– Rhegmatogenous, a bright red retinal break will also be visible. The tears

in rhegmatogenous retinal detachment usually occur in the superior half of the retina in a region of equatorial degeneration.

– Tractional retinal detachment, the bullous detachment will be accompanied by preretinal gray strands.

– Exudative retinal detachment, massive fatty deposits and often by intra retinal bleeding.

– The tumor-related retinal detachment secondary retinal detachment over the tumor or at some distance from the tumor in the inferior peripheral retina.

• Ultrasound studies can help confirm the diagnosis where retinal findings are equivocal or a tumor is suspected.

Rhegmatogenous

ExudateTractional

Treatment

• Retinal breaks with minimal circular retinal detachment can be treated with argon laser coagulation.

• Extensive retinal detachments are usually treated with a retinal tamponade with an elastic silicone sponge that is sutured to the outer surface of the sclera, a so called budding procedure.

• Rhegmatogenous RD — use reattachment surgery: laser, cryo-therapy plus explant or internal surgery with vitrectomy.

• Exudative and solid RD — establish and treat the cause.

• Tractional RD — relieve traction by vitreoretinal surgery

RETINAL VEIN OCCLUSION

• Vein occlusion occurs as a result of circulatory dysfunction in the central vein or one of its branches.

• Retinal vein occlusion is the second most frequent vascular retinal disorder after diabetic retinopathy and glaucoma.

Etiology

• Local thrombosis at sites where sclerotic arteries compress the veins.

• In central retinal vein occlusion, the thrombus lies at the level of the lamina cribrosa in branch retinal vein occlusion, it is frequently at an arteriovenous crossing.

Symptoms

• Patients only notice a loss of visual acuity if the macula or optic disk are involved.

Diagnostic

• Linear or punctiform hemorrhages are seen to occur in all four quadrants of t he retina.

• In branch retinal vein occlusion, intraretinal hemorrhages will occur in the area of vascular supply; this bleeding may occur in only one quadrant or in two quadrants (hemispheric vein occlusion).

• Cotton-wool spots and retinal or optic disk edema.• Chronic occlusions may also be accompanied by

lipid deposits.

Treatment

• In the acute stage of vein occlusion, hematocrit should be reduce d to 35 – 38 % by hemodilution.

• Laser treatment is performed in ischemic occlusion that progresses to neovascularization or rubeosis iridis.

• Focal laser treatment is performed in branch retinal vein occlusion with macular edema when visual acuity is re duce d to 20/40 or less within three months of occlusion.

RETINAL ARTERIAL OCCLUSION

• Retinal infarction due to occlusion of an artery in the lamina cribrosa or a branch retinal artery occlusion.

Etiology

• Emboli are frequently the cause of retinal artery and branch retinal artery occlusions.

• Less frequent causes include inflammatory processes such as temporal arteritis (Horton’s arteritis).

Symptoms

• Patient generally complains of sudden, painless unilateral blindness.

• In branch retinal artery occlusion, the patient will notice a loss of visual acuity or visual field defects.

Diagnostic

• In the acute stage of central retinal artery occlusion , the retina appears grayish white due to edema of the layer of optic nerve fibers and is no longer transparent.

• Fovea centralis, remains visible as a “ cherry red spot ” because the red of the choroid shows through at this site.

• Atrophy of the optic nerve will develop in the chronic stage of central retinal artery occlusion

Treatment

• Medications that reduce intraocular pressure, or paracentesis are applied in an attempt to drain t he embolus in a peripheral retinal vessel.

• Calcium antagonists or hemodilution are applie d in an attempt to improve vascular supply.

• Lysis therapy is no longer performed due to the poor prognosis (it is not able to prevent blindness) and the risk to vital tissue involved

VITREOUS HEMORRHAGE

• Bleeding into the vitreous chamber or a space created by vitreous detachment.

Etiology

• Bleeding from normal retinal vessels as can occur as a result of mechanical vascular damage in acute vitreous detachment or retinal tear.

• Bleeding from retinal vessels with abnormal changes as can occur as a result of retinal neovascularization in ischemic retinopathy or retinal macroaneurysms.

• Influx of blood from the retina or other sources such as the subretinal space or the anterior s egments of the eye.

• More frequent causes of vitreous hemorrhage include:– Posterior vitreous detachment with or without retinal tears

( 38 %).– Proliferative diabetic retinopathy (32 %).– Branch retinal vein occlusion ( 11 %).– Age-related macular degeneration (2 %).– Retinal macroaneurysm (2 %).

• Less frequent causes of vitreous hemor rhage include:– Arteriosclerosis.– Retinal periphlebitis.

Symptoms

• Patients often report the sudden occurrence of black opacities that they may describe as “ swarms of black bugs ” or “ black rain .”

• Severe vitreous hemorrhage can significantly reduce visual acuity Approximately 10 µl of blood are sufficient to reduce visual acuity to perception of hand movements in front of the eye.

Diagnostic

• Hemorrhages into the vitreous body itself do not exhibit any characteristic limitations but spread diffusely (the blood cannot form a fluid meniscus in the gelatinous vitreous body) and coagulation occurs quickly.

Treatment

• Patients with acute vitreous hemorrhage should be placed in an upright resting position.

• Next the cause of the vitreous hemorrhage should be treated, for example a retinal tear may be treate d with a laser.

• Vitrectomy will be require d to drain any vitreous hemorrhage that is not absorbed.

ANTERIOR ISCHEMIC OPTIC NEUROPATHY (AION)

Anterior Ischemic Optic Neuropathy (AION)

• The following forms of anterior ischemic optic neuropathy (AION) are distinguished according to the cause of the disorder:

1. Arteriosclerotic anterior ischemic optic neuropathy.

2. Arteritic anterior ischemic optic neuropathy.

1. Arteriosclerotic anterior ischemic optic neuropathy.

• An acute disruption of the blood supply to the optic disk, i.e., optic disk infarction, resulting from vascular changes in arteriosclerosis.

• Epidemiology: Arteriosclerotic AION is a common cause of sudden loss of visual acuity. The greatest incidence of this disorder is between the ages of 60 and 70. In contrast to arteritic AION, it can also occur in adults below the age of 60.

• Etiology: The causes of the disorder lie in acute disruption of the blood flow through the lateral branches of the short posterior ciliary arteries and the ring of Zinn in the setting of severe arteriosclerosis.

• Symptoms: Patients report a sudden unilateral loss of visual acuity. This is due to segmental or complete infarction of the anterior portion of the optic nerve.

• Severity is variable. The patient may present with wedge-shaped visual field defects or horizontal visual field defects that correlate with segmental nerve fiber edemas.

• However, severe concentric defects progressing to total blindness can also occur.

• Diagnostic considerations: The patient will frequently have a history of hypertension, diabetes mellitus, or hyperlipidemia.

• Ophthalmoscopy will reveal edema of the optic disk, whose margin will be accordingly obscured.

• Treatment: Examination by an internist and Doppler ultrasound studies of the carotid artery may be helpful because the diagnosis of the underlying cause is important

• Underlying disorders such as diabetes mellitus or arterial hypertension should be treated.

• Anterior ischemic optic neuropathy is nearly impossible to treat. Attempted methods include hemodilution (pentoxifylline infusions, acetyl-salicylic acid, and bloodletting depending on hematocrit levels) and systemic administration of steroids to control the edema.

• Prognosis: The prognosis is usually poor even where therapy is initiated early. Isolated atrophy of the optic nerve will appear within three weeks, complex atrophy of the optic nerve is less frequent but may also be observed.

2. Arteritic Anterior Ischemic Optic Neuropathy

• An acute disruption of the blood supply to the optic disk due to inflammation of medium-sized and small arterial branches.

• Epidemiology: The annual incidence is approximately three cases per 100000. The disorder occurs almost exclusively after the age of 60. Women are affected slightly more often than men, accounting for 55% of all cases.

• Etiology: Giant cell arteritis is a frequently bilateral granulomatous vasculitis that primarily affects the medium-sized and small arteries.

• Common sites include the temporal arteries, ophthalmic artery, short posterior ciliary arteries, central retinal artery, and the proximal portion of the vertebral arteries, which may be affected in varying combinations.

• Symptoms: Patients report sudden unilateral blindness or severe visual impairment. Other symptoms include headaches, painful scalp in the region of the temporal arteries, tenderness to palpation in the region of the temporal arteries, pain while chewing (a characteristic sign), weight loss, reduced general health and exercise tolerance.

• Patients may have a history of amaurosis fugax or polymyalgia rheumatica.

• Diagnostic considerations: The ophthalmoscopic findings are the same as in arteriosclerotic AION.

• Other findings include a significantly increased erythrocyte sedimentation rate/ESR (precipitous sedimentation is the most important hematologic finding), an increased level of C-reactive protein/CRP, leukocytosis, and iron-deficiency anemia.

• The temporal arteries are prominent , painful to palpation, and have no pulse. The diagnosis is confirmed by a biopsy of the temporal artery.

• Treatment: Immediate high-dosage systemic steroid therapy (initial doses up to 1000 mg of intravenous prednisone) is indicated. Steroids are reduced as the erythrocyte sedimentation rate decreases, C-reactive protein levels drop, and clinical symptoms abate.

• However, a maintenance dose will be required for several months. Vascular treatment such as pentoxifylline infusions may be attempted.

• Prognosis: The prognosis for the affected eye is poor even where therapy is initiated early. Immediate steroid therapy is absolutely indicated because in approximately 75% of all cases the fellow eye is affected within a few hours and cerebral arteries may also be at risk.

CENTRAL SEROUS CHORIORETINOPATHY

Central Serous Chorioretinopathy

• Serous detachment of the retina and/or retinal pigment epithelium.

• Etiology: Serous detachment occurs through a defect in the outer blood – retina barrier (“tight junctions” in the retinal pigment epithelium).

• Epidemiology: The disorder primarily affects men in the third and fourth decade of life.

• Symptoms: Patients present with a loss of visual acuity, a relative central scotoma (dark spot), image distortion, or perception of objects as larger or smaller than they are (macropsia or micropsia).

• Diagnostic considerations: Ophthalmoscopy will reveal a serous retinal detachment, usually at the macula. In chronic cases, a fine brown and white pigment epithelial scar will develop at the site of the fluid effusion.

• Swelling in the central retina shortens the visual axis and produces hyperopia.

• The site of fluid effusion can be identified during the active phase with the aid of fluorescein angiography

• Treatment: Usually no treatment is required for the first occurrence of the disorder. Retinal swelling resolves spontaneously within a few weeks. Recurrences may be treated with laser therapy provided the site of fluid effusion lies outside the fovea centralis.

• Clinical course and prognosis: The prognosis is usually good. However, recurrences or chronic forms can lead to a permanent loss of visual acuity.

CHOROIDITIS

Choroiditis

• Epidemiology: There are few epidemiologic studies of choroiditis. The annual incidence is assumed to be four cases per 100 000 people.

• Etiology:o Toxoplasmosiso Syphiliso Behçet’s diseaseo Trauma o Immunodeficiency o Post-surgery

• Symptoms: Patients are free of pain, although they report blurred vision and floaters.

• Diagnostic considerations: Ophthalmoscopy reveals isolated or multiple choroiditis foci. In acute disease they appear as ill-defined white dots. Once scarring has occurred the foci are sharply demarcated with a yellowish-brown color. Occasionally the major choroidal vessels will be visible through the atrophic scars.

• Treatment: Choroiditis is treated either with antibiotics or steroids, depending on its etiology.

• Prognosis: The inflammatory foci will heal within two to six weeks and form chorioretinal scars. The scars will result in localized scotomas that will reduce visual acuity if the macula is affected.

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